SA LMN Disease Flashcards

1
Q

what are 5 clinically important acute LMN diseases?

A
  1. tick paralysis
  2. polyradiculoneuritis
  3. myasthenia gravis
  4. myositis
  5. botulism
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2
Q

describe tick paraylsis

A
  1. neurotoxin from Dermacentor variables and andersoni ticks binds to presynapthic vesicles and inhibits Ach release
  2. clinical signs: dishrag, LMN!
    -5-7 days after tick infestation
    -rapid progression (24-48 hours)/acute onset
    -ascending weakness: pelvic to thoracic limbs
    –decreased tone, decreased to absent reflexes, loose and floppy
    -cranial nerves are rarely affected! if it does is usually just palpebral reflex
    -remove tick and use insectiCIDAL drugs!!
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3
Q

describe ascending canine polyradiculoneuritis/coonhoud paralysis

A
  1. looks like tick paralysis! acute onset, pelvic to thoracic
  2. pathology: inflammation of spinal roots; ventral or dorsal
  3. used to be called coonhound paralysis; potentially due to raccoon saliva but most of the time is idiopathic
    -in people, guillian barre: idiopathic secondary to antibodies against campylobacter
    -most dogs who have it are found to be eating raw chicken, which contains campylobacter
  4. disease of exclusion! if already treated for tick paralysis and didn’t work and have raw chicken in diet, consider this
  5. clinical signs: generalized weakness
    -cranial nerves rarely affected! if so, usually only facial paralysis (CN VII)
    -hyperesthesia (increased response to stimulus) in 25% of cases!
    -muscle atrophy with time!
  6. no great fix; will get better on its own once immune rxn dies down
    -supportive care while wait days to weeks to months
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4
Q

describe myasthenia gravis

A
  1. disease involving neuromuscular transmission
    -congenital (rare): abnormal AChR
    -acquired (most common): immune mediated autoantibodies directed against AchR, resulting in lack of AchR in skeletal muscle
  2. acquired form can be
    -primary: idiopathic
    -secondary: thymoma or cats with methimazole!
  3. breed predilection in comparison to mixed breeds!
    -if see diffuse neuromuscular, and rule out other things, look up and see if there is a breed predilection!
  4. predisposing causes
    -idiopathic: young to middle aged
    -paraneoplastic: older; thymoma or variety of other neoplasm (take thoracic radiographs to r/o thymoma!)
    -drugs: methimazole in cats!
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5
Q

describe clinical signs and presentations of myastenia gravis

A
  1. clinical signs:
    -EPISODIC exercise intolerance: worsens with exercise, improves with rest
    -preserved reflexes: palpebral reflex and patellar reflex!!
    -NO muscle atrophy
    -cranial nerves: facial, pharyngeal/laryngeal
    regurgitation! due to megaesophagus; you have to ask this, owner can’t tell vomit versus regurg
  2. two presentations:
    -generalized/appendicular weakness: all limbs affected with pharyngeal and esophageal dysfunction
    -focal: facial and pharyngeal weakness, esophageal
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6
Q

describe diagnosis and treatment of myastenia gravis

A

diagnosis:
-start with suspicious clinical signs
-chest rads (left and right lateral!!) to look for thymoma or megaesophagus or aspiration pneumonia
-neostigmine challenge: blocks acetylcholine esterase (like giving Ach); if dog gets better = much more suspicious for myastenia
-definitive: anti-Ach receptor antibodies: if have, have myastenia gravis!

treatment:
-cholinergic therapy: pyridostigmine bromide, neostigmine
-treat underlying cause: thymectomy for thymoma
-+/- immunosuppression, plasmapharesis
-upright feeding if megaesophagus
-for idiopathic: treat until stop producing antibodies (approx 6 months) and then wean off drug to see if return to normal once titers zero

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7
Q

describe botulism

A
  1. clostridium botulinum makes the toxin, which gets absorbed from GI tract after consumption of carrion or improperly made silage
  2. at NMJ, toxin binds to presynaptic nerve terminal and inhibits release of Ach
  3. clinical signs: nose to tail affects EVERYTHING
    -generalized weakness: facial, pharyngeal/laryngeal, appendicular, anal sphincter, tail
  4. treatment:
    -supportive care
    -antitoxin: ineffective when clinical signs are evident bc toxin already bound and within the nerve terminal!
    -also in dogs and cats is usually type C and antitoxin doesn’t even work on that type
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8
Q

describe diagnostics for chronic problems

A
  1. neuro exam
  2. minimun database:
    -CBC, chem, UA, CK
  3. +/- test for infectious disease
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9
Q

describe electrodiagnostics

A

also called electromyography/nerve conduction studies

measure electrical potential of extracellular environment to look at electrical activity of nerves in muscles

should have relatively large amplitudes over short amount of time

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10
Q

describe geriatric onset laryngeal paralysis (GOLP)

A
  1. labs (large/giant); also goldens, irish setters, newfies >9 years old
  2. many progress with 1 year and often have a poor withdrawal
  3. laryngeal paralysis is often the first sign!
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11
Q

describe diagnosis and treatment of GOLP

A

diagnosis: signalment, history, exam; exclusion of other causes

treatment:
-no specific (degeneration of axons)
-may need to address laryngeal paralysis surgically

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12
Q

describe nongeriatric laryngeal paralysis

A

can be congenital or inherited; will see with multiple in one litter of puppies

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13
Q

why are metabolic causes of chronic LMN disease the most important to consider? describe diagnosis and treatment

A
  1. easiest to diagnose
  2. easiest to treat
  3. most likely to improve

diagnosis:
-signalment, history, exam
-CBC, chemistry profile, urinalysis
–specialized tests (endocrine)
-exclusion of other causes

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14
Q

describe steroid myopathy

A
  1. exogenous (gave steroids) or endogenous (produce too much)
  2. signs of cushing’s disease/hyperadrenocorticism:
    -PU/PD, panting, restless
    -poor hair coat bilaterally along flank
    -pot bellied appearance
  3. muscle atrophy:
    -temporalis/masseter
    -generalized: axial muscles
    -pseudomyotonia: look stiff!
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15
Q

describe diabetes mellitus

A

clinical signs:
1. PU/PD/PP
2. weight loss
3. scruffy hair coat; dandruff!

classical presentation: plantigrade stance in cats!
-progressive pelvic limb lameness in dogs

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16
Q

describe what hypokalemia can result in

A

clinical signs:
1. low potassium, increased CK when potassium below 2.3 mEq/L, rhabdomyolysis when potassium below 2.0 mEq/L
2. neck flexion
3. generalized weakness; acute onset tetraparesis

treatment:
1. treat underlying cause
2. support renal tubular flow

17
Q

what are clinical signs of myositis?

A
  1. generalized neuromuscular disease
  2. serum chemistry:
    -CK elevation
    -AST
    -ALT
  3. differentials:
    -infectious: protozoal (neospora, toxoplasma, hepatozoan caninum, sarcocystic) can check with serology but problematic bc antibodies just = exposure
    -metabolic: hypothyroid, hypokalemic, endocrine
    -degenerative: muscular dystrophies
    -toxic
    -neoplasia